TY - JOUR
T1 - The impact of dietary fermentable carbohydrates on a postinflammatory model of irritable bowel syndrome
AU - Tuck, Caroline J.
AU - Caminero, Alberto
AU - Jiménez Vargas, Nestor N.
AU - Soltys, Carmen L.
AU - Jaramillo Polanco, Josue O.
AU - Lopez Lopez, Cintya D.
AU - Constante, Marco
AU - Lourenssen, Sandra R.
AU - Verdu, Elena F.
AU - Muir, Jane G.
AU - Lomax, Alan E.
AU - Reed, David E.
AU - Vanner, Stephen J.
PY - 2019/10/1
Y1 - 2019/10/1
N2 - Background: A low fermentable carbohydrate (FODMAP) diet is used in quiescent inflammatory bowel disease when irritable bowel syndrome-like symptoms occur. There is concern that the diet could exacerbate inflammation by modifying microbiota and short-chain fatty acid (SCFA) production. We examined the effect of altering dietary FODMAP content on inflammation in preclinical inflammatory models. Methods: C57BL/6 mice were given 3% dextran sodium sulfate (DSS) in drinking water for 5 days and recovered for 3 weeks (postinflammatory, n = 12), or 5 days (positive-control, n = 12). Following recovery, DSS-treated or control mice (negative-control, n = 12) were randomized to 2-week low- (0.51 g/100 g total FODMAP) or high-FODMAP (4.10 g) diets. Diets mimicked human consumption containing fructose, sorbitol, galacto-oligosaccharide, and fructan. Colons were assessed for myeloperoxidase (MPO) activity and histological damage. Supernatants were generated for perforated patch-clamp recordings and cytokine measurement. Cecum contents were analyzed for microbiota, SCFA, and branched-chain fatty acids (BCFA). Data were analyzed by two-way ANOVA with Bonferroni. Key results: Inflammatory markers were higher in the positive-control compared with negative-control and postinflammatory groups, but no differences occurred between the two diets within each treatment (MPO P >.99, histological scores P >.99, cytokines P >.05), or the perforated patch-clamp recordings (P >.05). Microbiota clustered mainly based on DSS exposure. No difference in SCFA content occurred. Higher total BCFA occurred with the low-FODMAP diet in positive-control (P <.01) and postinflammatory groups (P <.01). Conclusions and inferences: In this preclinical study, reducing dietary FODMAPs did not exacerbate nor mitigate inflammation. Microbiota profile changes were largely driven by inflammation rather than diet. Low FODMAP intake caused a shift toward proteolytic fermentation following inflammation.
AB - Background: A low fermentable carbohydrate (FODMAP) diet is used in quiescent inflammatory bowel disease when irritable bowel syndrome-like symptoms occur. There is concern that the diet could exacerbate inflammation by modifying microbiota and short-chain fatty acid (SCFA) production. We examined the effect of altering dietary FODMAP content on inflammation in preclinical inflammatory models. Methods: C57BL/6 mice were given 3% dextran sodium sulfate (DSS) in drinking water for 5 days and recovered for 3 weeks (postinflammatory, n = 12), or 5 days (positive-control, n = 12). Following recovery, DSS-treated or control mice (negative-control, n = 12) were randomized to 2-week low- (0.51 g/100 g total FODMAP) or high-FODMAP (4.10 g) diets. Diets mimicked human consumption containing fructose, sorbitol, galacto-oligosaccharide, and fructan. Colons were assessed for myeloperoxidase (MPO) activity and histological damage. Supernatants were generated for perforated patch-clamp recordings and cytokine measurement. Cecum contents were analyzed for microbiota, SCFA, and branched-chain fatty acids (BCFA). Data were analyzed by two-way ANOVA with Bonferroni. Key results: Inflammatory markers were higher in the positive-control compared with negative-control and postinflammatory groups, but no differences occurred between the two diets within each treatment (MPO P >.99, histological scores P >.99, cytokines P >.05), or the perforated patch-clamp recordings (P >.05). Microbiota clustered mainly based on DSS exposure. No difference in SCFA content occurred. Higher total BCFA occurred with the low-FODMAP diet in positive-control (P <.01) and postinflammatory groups (P <.01). Conclusions and inferences: In this preclinical study, reducing dietary FODMAPs did not exacerbate nor mitigate inflammation. Microbiota profile changes were largely driven by inflammation rather than diet. Low FODMAP intake caused a shift toward proteolytic fermentation following inflammation.
KW - di-
KW - dietary therapy
KW - fermentable oligo-
KW - fermentation patterns
KW - inflammation
KW - mono-saccharides and polyols
UR - http://www.scopus.com/inward/record.url?scp=85068710207&partnerID=8YFLogxK
U2 - 10.1111/nmo.13675
DO - 10.1111/nmo.13675
M3 - Article
C2 - 31290223
AN - SCOPUS:85068710207
SN - 1350-1925
VL - 31
JO - Neurogastroenterology & Motility
JF - Neurogastroenterology & Motility
IS - 10
M1 - e13675
ER -
